Therapeutic effects of the Qingre-Qushi recipe on atopic dermatitis through the regulation of gut microbiota and skin inflammation
Therapeutic effects of the Qingre-Qushi recipe on atopic dermatitis through the regulation of gut microbiota and skin inflammation
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DOI：
10.1016/j.heliyon.2024.e26063
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发表时间：
2024-02-13
期刊：
影响因子：
4
通讯作者：
Ma，Xin
中科院分区：
文献类型：
--
作者：
Shen，Fang;Gao，Chunjie;Ma，Xin
越来越多的证据强调肠道微生物群与特应性皮炎 (AD) 的发生、发展、预防和治疗之间存在密切关联。通过口服中药调节肠道微生物失调已引起人们的广泛关注。在治疗AD方面，中药清热祛湿方（QRQS）已显示出临床疗效。然而，QRQS 的治疗机制及其对肠道微生物群的影响仍不清楚。因此，我们的研究旨在评估 QRQS 的功效并评估其对 AD 动物模型肠道微生物群组成和多样性的影响。首先，我们使用两种动物模型研究了 QRQS 对 AD 的治疗效果：丝聚蛋白缺陷小鼠（Flaky tail，ft/ft）和 MC903 诱导的 AD 样小鼠。随后，我们探讨了它对肠道微生物群组成和多样性的影响。我们的结果表明，QRQS 治疗可改善 ft/ft 小鼠和 MC903 诱导的 AD 样小鼠的症状。它还降低了血清 IgE 和促炎细胞因子的水平，包括 IL-1β、IL-4、IL-5、IL-9、IL-13、IL-17A 和 TNF-α。此外，QRQS 通过增加乳杆菌科和减少拟杆菌科来显着调节肠道微生物群多样性。根据 Spearman 相关系数确定，ft/ft 小鼠外周血清中的炎症因子与肠道微生物群密切相关。此外，PICRUSt 分析显示，与 ft/ft 组相比，QRQS 组的抗坏血酸和丙二酸代谢、脂肪酸代谢和生物合成以及丙酸代谢有所丰富。最后，我们使用超高效液相色谱-高分辨率质谱（UPLC-HRMS）确定甘草苷是 QRQS 的主要活性成分。我们的研究结果表明，QRQS 改善了 ft/ft 和 MC903 诱导小鼠的 AD 样症状并减轻了皮肤炎症。这表明调节肠道菌群可能有助于阐明其抗炎激活机制，突出了一种针对肠道菌群预防和治疗 AD 的新治疗策略。
Accumulating evidence has highlighted a strong association between gut microbiota and the occurrence, development, prevention, and treatment of atopic dermatitis (AD). The regulation of gut microbial dysbiosis by oral traditional Chinese medicine (TCM) has garnered significant attention. In the treatment of AD, the TCM formula Qingre-Qushi Recipe (QRQS) has demonstrated clinical efficacy. However, both the therapeutic mechanisms of QRQS and its impact on gut microbiota remain unclear. Thus, our study aimed to assess the efficacy of QRQS and evaluate its influence on the composition and diversity of gut microbiota in AD animal models. First, we investigated the therapeutic effect of QRQS on AD using two animal models: filaggrin-deficient mice (Flaky tail, ft/ft) and MC903-induced AD-like mice. Subsequently, we explored its influence on the composition and diversity of gut microbiota. Our results demonstrated that QRQS treatment ameliorated the symptoms in both ft/ft mice and MC903-induced AD-like mice. It also reduced the levels of serum IgE and pro-inflammatory cytokines, including IL-1β, IL-4, IL-5, IL-9, IL-13, IL-17A, and TNF-α. Furthermore, QRQS remarkably regulated gut microbiota diversity by increasingLactobacillaceaeand decreasingBacteroidales. The inflammatory factors in peripheral serum of ft/ft mice showed a close correlation with gut microbiota, as determined using the Spearman correlation coefficient. Additionally, PICRUSt analysis revealed an enrichment in ascorbate and aldarate metabolism, fatty acid metabolism and biosynthesis, and propanoate metabolism in the QRQS group compared to the ft/ft group. Finally, we identified liquiritin as the primary active ingredient of QRQS using ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UPLC-HRMS). Our findings revealed that QRQS improved AD-like symptoms and alleviated skin inflammation in ft/ft and MC903-induced mice. This suggests that modulating the gut microbiota may help elucidate its anti-inflammation activation mechanism, highlighting a new therapeutic strategy that targets the intestinal flora to prevent and treat AD.